First Aid - Respiratory - Physiology

Front 1

surfactant - dipalmitoyl phosphatidylcholine (DPPC) (lecithin)

Back 1

produced by type II pneumocytes (3%) of all pneumocytes - decreases the surface tension of alveoli, increases compliance and decreases the work of inspiration
*prevents atelectasis (collapse of a lung)

Front 2

What is deficient in neonatal RDS?

Back 2

surfactant (DPPC) - lecithin

Front 3

What are important lung products?

Back 3

1. surfactant - increases compliance, decreases surface tension, decreases work of inspiration
2. prostaglandins
3. Histamine - increase bronchoconstriction
4. ACE - converts AT I to AT II; inactivates bradykinin (ace inhibitors increase bradykinin and produce angioedema and cough)
5. Kallikrein - activates bradykinin

Front 4

What creates a tendency for the lung to collapse?

Back 4

decreased radius on expiration
collapsing pressure = 2(tension)/radius

Front 5

What does surface tension do to the alveoli? What does the radius of the alveoli do?

Back 5

surface tension tries to collapse the alveoli while the radius tries the keep the alveoli open
collapsing pressure = 2(surface tension)/radius

*when the radius decreases during expiration - have increased risk of alveolar collapse

Front 6

Residual volume

Back 6

volume left in the lungs - after maximal expiration (cannot be measured with spirometry)

Front 7

What lung volumes cannot be measured by spirometry?

Back 7

RV, TLV, FRC

Front 8

Expiratory reserve volume (ERV)

Back 8

air that can be still breathed out after a normal expiration

Front 9

Tidal volume

Back 9

air that moves in and out of the lungs during a normal breath (usually around 500 mL)

Front 10

What normally is the tidal volume?

Back 10

500mL (air that moves in and out of the lungs during a normal breath)

Front 11

Inspiratory reserve volume (IRV)

Back 11

volume that can still be inspired after normal breath in.
(air in excess of tidal volume that moves into the lung on maximal inspiration

Front 12

Vital capacity

Back 12

amount of air moved in biggest inspiration and biggest expiration (TV + ERV + IRV

Front 13

Functional residual capacity (FRC)

Back 13

volume in lungs after a normal expiration
(RV + ERV)

Front 14

Inspiratory capacity (IC)

Back 14

IRV + TV

Front 15

total lung capacity

Back 15

maximal amount of air someone can breathe in and out (including what is left over)
RV + ERV + TV + IRV

Front 16

What is the pysiologic dead space?

Back 16

anatomical dead space of conducing airways plus functional dead space in alveoli; apex of healthy lung is largest contributor of functional dead space. Volume of inspired air that does not participate in gas exchange

Front 17

What part of a healthy lung contributes the most to the functional dead space?

Back 17

apex of a healthy lung

Front 18

What do the lung and chest wall want to do independent of each other?

Back 18

lung wants to collapse
chest wall wants to expand

Front 19

What is it when the inward pull of the lung is balanced with the outward pull of the chest wall?

Back 19

FRC - system pressure is atmospheric

Front 20

what determines the combined volume of the lung and the chest wall?

Back 20

elastic properties of both chest wall and lung

Front 21

What is hemoglobin composed of?

Back 21

4 polypeptide subunits (2a and 2B) each subunit has heme group (Fe + porphyrin ring)

Front 22

What are the states the globin chains exist in?

Back 22

1) T (taut) form has low affinity for O2
2) R (relaxed) form has high affinity for O2 (300x). Hemoglobin exhibits positive cooperativity and negative allostery (accounts for sigmoid shaped O2 dissociation curve for hemoglobin unlike myoglobin)

Front 23

What does an increase in Cl-, H+, CO2, 2,3 BPG and temperature do to hemoglobin?

Back 23

changes the R hemoglobin form into T hemoglobin form - shifts dissociation curve to the right - increased unloading of O2 in the tissues

Front 24

what does modification of hemoglobin lead to?

Back 24

tissue hypoxia from decreased O2 saturation and decreased O2 content

Front 25

What is methemoglobin?

Back 25

oxidized form of hemoglobin (ferric, Fe3+) that does not bind O2 as readily, but has increased affinity for CN- (cyanide)
Iron in hemoglobin is normally in a reduced form (ferrous, Fe2+)

Front 26

What form is iron usually in in hemoglobin?

Back 26

ferrous (reduced form, Fe2+)

Front 27

What form is iron in in methemoglobin?

Back 27

ferric (oxidized form, Fe3+)

Front 28

What do you do to treat cyanide poisoning?

Back 28

use nitrates to oxidize hemoglobin to methemoglobin, which binds cyanide, allowing cytochrome oxidase to function. Use thiosulfate to bind this cyanide, forming thiocynate, which is renally excreted

Front 29

What can you use to treat methemoblobinemia

Back 29

methylene blue

Front 30

What 2 things do you give to treat cyanide poisoning?

Back 30

first give nitrates to oxidize iron to form methemoglobin
then give thiosulfate to bind this cyanide to form thiocynate - which will be renally excreted

Front 31

What causes the sigmoidal shape of the oxygen-hemoglobin dissociation curve?

Back 31

positive cooperativity - hemoglobin can bind 4 oxygen - after one binds - increased affinity for next one and even more affinity for following one

Front 32

What does a right shift in the oxygen - hemoglobin dissociation curve mean?

Back 32

Hemoglobin has a decreased affinity for oxygen - facilitates unloading of O2 at the tissues

Front 33

What causes a right shift in the oxygen-hemoglobin dissociation curve?

Back 33

CADET - all of these increased (except pH) causes right shift of curve
CO2 (increased)
Acid/altitude
DPG (2,3 BPG)
Exercise
Temperature (increase)

Front 34

What does fetal hemoglobin do to the oxygen-hemoglobin dissociation curve?

Back 34

causes a left shift - increased affinity for O2 (the fetal hemoglobin)

Front 35

An increase in pH shifts the oxygen-hemoglobin dissociation curve which direction?

Back 35

to the left

Front 36

Perfusion limited substances

Back 36

O2 (normal health), CO2, N2O - gas equilibrates early along the length of the capillary. Diffusion can only bee increased if blood flow increases

Front 37

diffusion limited substances

Back 37

O2 (emphysema, fibrosis), CO
gas goes not equilibrate by the time blood reaches the end of the capillaries

Front 38

Describe pulmonary circulation

Back 38

normally a low-resistance, high compliance system. PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation. A decrease in PAO2 (low pressure of O2 in the alveolus) causes hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of the lung to well-ventilated regions of the lung

Front 39

What is a consequence of pulmonary hypertension?

Back 39

cor pulmonale and subsequent right ventricular failure (jugular venous distention, edema, hepatomegly)

Front 40

What is characteristic of pulmonary hypertension?

Back 40

normal pulmonary artery pressure = 10-14 mmHG; pulmonary hypertension >25 mm Hg or >35 mmHg during exercise
*results in athersclerosis, medial hypertrophy and intimial fibrosis of pulmonary arteries

Front 41

What causes primary pulmonary hypertension?

Back 41

inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation); poor prognosis

Front 42

inactivating mutation in BMPR2 gene causes what?

Back 42

primary pulmonary hypertension - get vascular smooth muscle proliferation - bad prognosis

Front 43

What causes secondary pulmonary hypertension?

Back 43

COPD (destruction of lung parenchyma); mitral stenosis (increased resistance - increased pressure), recurrent trhomboemboli (decreased cross-sectional area of pulmonary vasculature bed; autoimmune disease (systemic sclerosis, inflammation - intimal fibrosis - medial hypertrophy); left to right shunt (increased shear stress - endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction)

Front 44

What is the course of illness with someone with secondary pulmonary hypertension?

Back 44

severe respiratory distress - cyanosis and RVH - death from decompensated cor pulmonale

Front 45

What is the equation for pulmonary vasculature resistance?

Back 45

PVR = (pul artery - Platrium)/CO

change in pressure between the pulmonary artery and the L atrium all divided by cardiac ouput

Front 46

What is the equation for oxygen content of blood?

Back 46

O2 content = (O2 binding capacity x % saturation) + dissolved O2

O2 binding capacity = 20.1 mL O2/dL

Front 47

O2 delivery to the tissues equation?

Back 47

O2 delivery to the tissues = CO x O2 content of blood

Front 48

When does cyanosis result?

Back 48

When deoxygenated Hb > 5g/dL

Front 49

What is the normal binding capacity of O2?

Back 49

20.1 mL O2/dl
(used to calculate O2 content = (O2 binding capacity x %saturation) + dissolved O2

Front 50

What happens as Hg decreases?

Back 50

O2 content of arterial blood decrases, but O2 saturation and arterial P02 do not decrease

Front 51

What does decrease arterial PO2 in an individual?

Back 51

chronic lung disease because physiology shunt (when air is blocked from getting to the lungs ie piece of steak caught in the airway) decreases O2 extraction ratio

Front 52

What are the reasons for an increased A-a?

Back 52

hypoxemia caused by: shunt, diffusion block (fibrosis), V/Q mismatch

Front 53

What is the alveolar gas equation?

Back 53

PAO2 = PIO2 - (PACO2/R)
R = CO2 produced/O2 consumed
PAO2 - alveolar PO2
PaO2 - arterial PO2
PIO2 - PO2 of inspired air

Front 54

What is the A-a equation?

Back 54

PAO2 - PaO2

PAO2 is from the alveolar gas equation
PaO2 is from arterial blood

Front 55

Hypoxemia vs. Hypoxia

Back 55

hypoxemia (decreased PaO2)
hypoxia (decreased O2 delivery to tissues)

Front 56

What causes hypoxemia?

Back 56

decreased PaO2

high altitude (normal A-a gradient)
Hypoventilation (normal A-a gradient)
V/Q mismatch (increased A-a gradient)
Diffusion limitation (increased A-a gradient)
Right to left shunt (increased A-a gradient

Front 57

What causes hypoxia?

Back 57

decreased O2 delivery to tissues

decreased CO
hypoxemia
anemia
cyanide poisoning
CO poisoning

Front 58

What causes Ischemia?

Back 58

loss of blood flow

impeded arterial flow
reduced venous drainage

Front 59

Ischemia vs. hypoxia vs. hypoxemia

Back 59

ischemia - loss of blood flow
hypoxia - decreased O2 delivery to tissues
hypoxemia - decreased PaO2

Front 60

What is ideal for V/Q to equal?

Back 60

1 in order for adequate gas exchange to occur

Front 61

What happens to V and Q as you go from the apex to the base of the lungs (zone 1 to zone 3)?

Back 61

The both increase - but blood flow increases faster - so as you go from the apex to the base the V/Q gets lower (along with the PO2)

Front 62

What is zone 1 of the lung? What is characteristics of the area?

Back 62

apex of the lung - largest V/Q ratio - largest PO2 (reason why TB likes to go to the apex)

No blood flow - ventilation wasted - because PA>Pa>Pv (because the alveolar pressure is greater than arterial - little blood flow to this area of the lung)
V/Q is the largest (3)

Front 63

What zone of the lung has increased dead space?

Back 63

apex - because PA>Pa>Pv - so wasted ventilation

Front 64

What is zone 2 of the lung? What are characteristics of the lung?

Back 64

middle part - ventilation and perfusion both are increasing
Pa>PA>Pv - so are able to get blood flow to the area

Front 65

What happens to V and Q as you go from the apex to the base of the lungs (zone 1 to zone 3)?

Back 65

The both increase - but blood flow increases faster - so as you go from the apex to the base the V/Q gets lower (along with the PO2)

Front 66

What is zone 1 of the lung? What is characteristics of the area?

Back 66

apex of the lung - largest V/Q ratio - largest PO2 (reason why TB likes to go to the apex)

No blood flow - ventilation wasted - because PA>Pa>Pv (because the alveolar pressure is greater than arterial - little blood flow to this area of the lung)
V/Q is the largest (3)

Front 67

What is zone 3 of the lung? What are the characteristics of the area?

Back 67

base of the lung
Pa>Pv>PA - perfusion wasted
increased blood flow here because of recruitment and distention

Front 68

What zone of the lung has increased dead space?

Back 68

apex - because PA>Pa>Pv - so wasted ventilation

Front 69

As you go from the apex to the base what happens to V/Q? PO2? Ventilation? Perfusion?

Back 69

Ventilation and perfusion increase as you go from the apex to the base
V/Q and PO2 - decrease as you go from the apex to the base

Front 70

What is zone 2 of the lung? What are characteristics of the lung?

Back 70

middle part - ventilation and perfusion both are increasing
Pa>PA>Pv - so are able to get blood flow to the area

Front 71

What happens during exercise to the V/Q ratio?

Back 71

With exercise (increased CO), there is vasodilation of apical capillaries resulting in a V/Q that approaches 1 (decreases to 1) - because blood flow increases (Q)

Front 72

What is zone 3 of the lung? What are the characteristics of the area?

Back 72

base of the lung
Pa>Pv>PA - perfusion wasted
increased blood flow here because of recruitment and distention

Front 73

When V/Q = 0 what has happened?

Back 73

V = 0
shunt (piece of steak in the airway) - giving 100% O2 will NOT increase the PO2 because the airway is blocked

Front 74

As you go from the apex to the base what happens to V/Q? PO2? Ventilation? Perfusion?

Back 74

Ventilation and perfusion increase as you go from the apex to the base
V/Q and PO2 - decrease as you go from the apex to the base

Front 75

When V/Q = infinity what has happened?

Back 75

Q = 0
blood flow obstruction (physiologic dead space)
as long as there is not 100% dead space giving 100% O2 will improve the PO2

Front 76

What happens during exercise to the V/Q ratio?

Back 76

With exercise (increased CO), there is vasodilation of apical capillaries resulting in a V/Q that approaches 1 (decreases to 1) - because blood flow increases (Q)

Front 77

In what situation would giving 100% O2 improve the PO2?

Back 77

When V/Q = infinity
Q = 0
no blood flow (physiologic dead space)
as long as there is not 100% dead space giving 100% O2 would increase the PO2

Front 78

When V/Q = 0 what has happened?

Back 78

V = 0
shunt (piece of steak in the airway) - giving 100% O2 will increase the PO2 because the airway is blocked

Front 79

When V/Q = infinity what has happened?

Back 79

Q = 0
blood flow obstruction (physiologic dead space)
as long as there is not 100% dead space giving 100% O2 will improve the PO2

Front 80

In what situation would giving 100% O2 improve the PO2?

Back 80

When V/Q = infinity
Q = 0
no blood flow (physiologic dead space)
as long as there is not 100% dead space giving 100% O2 would increase the PO2

Front 81

What are the 3 ways CO2 is carried in the blood?

Back 81

1) 90% as bicarbonate - CO2 becomes hydrated (H20 added) forms H2CO3 (via Carbonic anhydrase) then can freely dissociate into H+ and HCO3-
2) Bound to hemoglobin at N terminus of globin (not heme) as carbaminohemoglobin (5%). CO2 binding favors taut form (O2 unloaded)
3) Dissolved CO2 (5%)

Front 82

Once the blood gets to the lungs what happens to the HCO3-?

Back 82

it goes back into the RBC via the Cl-/HCO3- transporter - in the RBC goes through the reactions to get CO2 which is then expired via the lungs

Front 83

What buffers H+ (produced from HCO3- and H+) inside the RBC until the blood gets to the lungs?

Back 83

H+ is buffered by deoxyhemoglobin (because H+ binds better to deoxyhemoglobin than oxyhemoglobin) so it is a good idea that Hg is in deoxyhemoglobin form by the time it reaches the venous end of the capillaries - because that is when CO2 is being added)

Front 84

What is the Haldane effect?

Back 84

In the lungs, oxygenation of hemoglobin - promotes the dissociation of H+ from the Hg - and favors the formation of CO2 - therefore CO2 is released from the RBC

Front 85

What is the Bohr effect?

Back 85

In peripheral tissue, increased H+ from tissue metabolism shifts the curve to the right, unloading O2

Front 86

What is the lung's response to high altitude?

Back 86

1) acute and chronic increase in ventilation
2) increased erythropoietin - increased hematocrit and hemoglobin (chronic hypoxia)
3) Increased 2,3 DPG (to right shift the curve) so hemoglobin releases more O2
4) cellular changes (increased mitochondria)
5) increased renal excretion of bicarbonate (can augment by use of acetazolamide) to compensate for respiratory alkalosis (resp alkalosis b/c hypoxemia stimulates peripheral chemoreceptors to increase ventilation rate - blow off more CO2 - become alkalotic)
6) Chronic hypoxic pulmonary vasoconstriction results in RVH

Front 87

What is the lung's response to exercise?

Back 87

1) Increased CO2 production and increased O2 consumption
2) increased ventilation rate to meet O2 demand
3) V/Q ratio from apex to base becomes more uniform (at apex approaches 1) - b/c Q increases from vasodilation
4) increased pulmonary blood flow because of increased CO
5) decreased pH during strenuous exercise (secondary to lactic acidosis) - no pH change during moderate exercise
6) No change in PaO2 and PaCO2, but increase in venous CO2 content (increase in venous CO2 because more CO2 is produced by exercising muscle and must be carried to the lungs to be expired)